At Emergency Nursing World
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End Tidal Carbon Dioxide Monitoring During CPR:
A Predictor of Outcome
by Jinhee Nguyen, RN MSN
Introduction
In the emergency department (ED), critical management of the patient’s
airway, ventilation and chest compression requires the utmost effort and
sophisticated technology to maximize successful outcomes. Approximately $1
billion is spent on emergency department and in-hospital care for cardiac
arrest nonsurvivors (Bonnin et al., 1993; Gray, Capone & Most, 1991). A
reliable method of assessing the efficacy and usefulness of ongoing
cardiopulmonary resuscitation (CPR) would conserve scarce health care
resources, avoid futile care, pain and suffering (Sanders, Kern, Otto,
Milander & Ewy, 1989; Wayne et al., 1995). End tidal carbon dioxide (ETCO2)
monitoring during resuscitation is a promising technology, which may help
maximize patient outcomes, while reducing futile and costly interventions.
ETCO2 is the partial pressure or maximal concentration of carbon dioxide
(CO2) at the end of an exhaled breath, which is expressed as a percentage
of CO2 or mmHg (LaValle & Perry, 1995; Santos, Varon, Pic-Aluas & Combs,
1993; Trillo, von Planta & Kette, 1994). The normal values are 5% to 6%
CO2, which is equivalent to 35-45 mmHg (Hollinger & Hoyt, 1995; Trillo et
al., 1994). CO2 reflects cardiac output (CO) and pulmonary blood flow as
the gas is transported by the venous system to the right side of the heart
and then pumped to the lungs by the right ventricles (LaValle & Perry,
1995; Sanders, 1989). When CO2 diffuses out of the lungs into the exhaled
air, a device called capnometer measures the partial pressure or maximal
concentration of CO2 at the end of exhalation (Sanders, 1989; Santos et
al., 1993). During CPR, the amount of CO2 excreted by the lungs is
proportional to the amount of pulmonary blood flow (Benumof, 1998; Lambert,
Cantineau, Merckx, Bertrand & Duvaldestine, 1992; Nielsen, Fitchet &
Saunders, 1990).
The primary interventions of CPR include establishing a patent airway,
ventilation, and precordial compressions. These interventions can help
maintain blood flow and oxygen delivery to the vital organs with a cardiac
output of about 17% to 27% (Falk, Rackow & Weil, 1988; Gudipati, Weil,
Bisera, Deshmukh & Rackow, 1988). During CPR, the most reliable continuous
monitoring of the efficacy of precordial compressions for blood flow is the
measurement of arterial or intracardiac pressure (Callaham & Barton, 1990;
Gudipati et al., 1988). Animal studies have reported the correlation of
coronary perfusion pressure (CPP) to the likelihood of resuscitation, but
simultaneous measurement of arterial pressure and central venous pressure
is required to monitor the progress of the resuscitation (Gudipati et al.,
1988; Sanders, Ewy, Bragg, Atlas & Kern, 1995). Furthermore, placing
catheters to measure such pressures is invasive, time consuming, and
impractical in the ED setting, especially when patient’s pulses are barely
palpable (Callaham & Barton, 1990; Gudipati et al., 1988; Sanders et al.,
1989). Therefore, ETCO2 monitoring is one promising noninvasive method of
evaluating patients, who are most likely to be intubated during CPR
(Cantineau et al., 1996; Lambert et al., 1992; Sanders et al., 1985;
Steedman & Robertson, 1990).
This paper will discuss the significance of ETCO2 monitoring and assess its
value in predicting the outcomes of CPR in ED and prehospital settings. The
inclusion of prehospital setting is crucial since the resuscitation from
the field is often continued in ED setting.
Significance
The current methods of assessing the effectiveness of CPR are difficult and
unreliable (Falk et al., 1988; Sanders et al., 1989; Santos et al., 1993).
The presence of femoral or carotid pulsations, pupillary signs, and
arterial blood gas (ABG) results have not shown to correlate with
successful CPR (Sanders et al., 1989; Santos et al., 1993; Steedman et al.,
1990). Currently, palpating pulses is one of the options for assessing the
adequacy of blood flow generated by cardiac compressions (Sanders et al.,
1989). According to Advanced Cardiac Life Support (ACLS) guidelines by
American Heart Association (1998), assessing for pulse is indicated before
confirming the return of spontaneous circulation (ROSC). However, a
palpable pulse may only represent continuity of a fluid filled vessel but
not necessarily the blood flow (Gudipati et al., 1988). Therefore, palpable
pulse may serve as an unreliable indication of operative systemic flow.
The most direct technique to measure the adequacy of ventilation is the
measurement of the partial pressure of carbon dioxide in arterial blood
(PaCO2) from an ABG, which can be expensive and painful (Santos et al.,
1993). During cardiac arrest, the CO2 delivery to the lungs decreases due
to poor pulmonary perfusion (Sanders et al., 1989). A decrease in pulmonary
blood flow will cause the accumulation of CO2 in the venous circuit even
with adequate ventilation (Steedman et al., 1990). CO2 delivery to the
lungs is decreased due to a high ventilation/perfusion (VQ) ratio, leading
to arterial alkalemia (Steedman et al., 1990; Weil, Rackow, Trevino,
Grundler, Falk, & Griffel, 1986). ABG’s can be misleading during CPR due to
a phenomenon called venous paradox, which consists of venous hypercarbic
acidosis and arterial hypocarbic alkalemia (Santos et al., 1993). In
addition, ABG’s only provide intermittent data, whereas capnometry allows
continuous and instantaneous measurement of ETCO2 (Santos et al., 1993).
The significance of ETCO2 monitoring during CPR was first noted by Kalenda
(1978), who observed the resuscitation of three patients and monitored
pulmonary perfusion by means of ETCO2. He reported that ETCO2 monitoring
was helpful in assessing rescuer exhaustion. With the external cardiac
massage, there was a slight improvement of ETCO2, which diminished as the
rescuer became tired. Replacing the fatigue rescuer with a fresh rescuer
resulted in an improvement in ETCO2. Additionally, Kalenda (1978) noted
that the sudden steep increase in ETCO2 was an indication of the return of
spontaneous cardiac activity. This study showed a potential significant
value of ETCO2 as a guiding tool to monitor the effectiveness of CPR.
Following the observation made by Kalenda (1978), several experimental
studies involving animals have demonstrated the correlation between ETCO2
with CO and CPP (Gudipati et al., 1988; Ornato, Garnett, & Glauser, 1990;
Sanders et al., 1985). The next series of in-hospital studies attempted to
confirm the same findings seen from experimental studies by looking at
ETCO2 monitoring during various hemodynamic stages of CPR in the ED. More
recent studies have used ETCO2 monitoring in prehospital settings in an
attempt to predict the outcome of CPR (Asplin & White, 1995; Cantineau et
al., 1996; Levine, Wayne & Miller, 1997; Wayne et al., 1995).
Organization of Review
The process of gathering the related literature was accomplished by
accessing the MEDLINE and CINAHL databases (1985-1999) at University of
California, San Francisco. The databases contained both medical and nursing
journals. The title word end tidal carbon dioxide in combination with two
key words, cardiac output and cardiopulmonary resuscitation, identified 18
articles. Majority of the articles were published by medical journals,
whereas only two articles were published by nursing journals (Benumof,
1998; LaValle & Perry, 1995). For the purpose of this paper, the articles
related to ED and prehospital settings were selected for in-depth discussion.
Discussion of Theory/Pathophysiology
To understand the significant value of ETCO2, one needs to be familiarized
with the following: normal physiology of CO2, principle determinants of
ETCO2, CO2 gradient with normal VQ relationship, ETCO2 analyzer
(capnometer), and limitations of ETCO2 measurements.
ETCO2 represents the partial pressure or maximal concentration of CO2 at
the end of exhalation (LaValle & Perry, 1995; Santos et al., 1993; Trillo
et al., 1994). CO2 reflects cellular metabolism (Idris et al., 1994;
Sanders, 1989). There are four main stages of normal physiology of CO2 :
production, transport, buffering and elimination. CO2 is a metabolic
byproduct of aerobic cell metabolism (LaValle & Perry, 1995; Sanders,
1989). As the intracellular CO2 increases, CO2 diffuses out into the tissue
capillaries and is carried by the venous circulation to the lungs, where it
diffuses from pulmonary capillaries into the alveoli (Idris et al., 1994;
LaValle & Perry, 1995). The partial pressure of CO2 (PaCO2) of venous blood
entering pulmonary capillaries is normally 45 mmHg; the partial alveolar
pressure of CO2 (PACO2) is normally 40 mmHg (LaValle & Perry, 1995; Trillo
et al., 1994). The pressure difference of 5 mmHg will cause all the
required CO2 to diffuse out of pulmonary capillaries into the alveoli
(LaValle & Perry, 1995). The second stage is CO2 transport, which is a way
of maintaining the CO2 tension of arterial blood at approximately 35-45
mmHg despite high CO2 production (Trillo et al., 1994).
The third stage is where the buffer action of hemoglobin and pulmonary
blood flow maintain the normal level of CO2 tension by eliminating the
excess CO2 (Trillo et al., 1994). CO2 can either be carried, dissolved or
combined with water (H20) to form carbonic acid (H2CO3), which can
dissipate to hydrogen ions (H+) and bicarbonate ions (HCO3-): (CO2 + H20 «
H2CO3 « H+ + HCO3-) (LaValle & Perry, 1995; Trillo et al., 1995). The
hydrogen ions are buffered by hemoglobin, and the bicarbonate ions are
transported into the blood (Idris et al., 1994; Trillo et al., 1994). This
mechanism accounts for 90% of CO2 transport (LaValle & Perry, 1995; Trillo
et al., 1994). The fourth stage involves CO2 elimination by alveolar
ventilation under the control of the respiratory center (LaValle & Perry,
1995; Trillo et al., 1994). This process allows the diffusion of CO2 from
blood to the alveoli where the partial alveolar pressure of CO2 is lower
than the tissue pressure (Trillo et al., 1994).
During normal circulatory condition with equal VQ relationship, PACO2 is
closely comparable to PaCO2 and ETCO2; therefore, PaCO2 is equivalent to
ETCO2 (Sanders, 1989; Santos et al., 1993). The difference between PaCO2
and ETCO2 is known as the CO2 gradient (LaValle & Perry, 1995). The normal
ETCO2 is about 38 mmHg at 760 mmHg of atmosphere with less then 6 mmHg
gradient between PaCO2 and ETCO2 (Sanders, 1989; Santos et al., 1993).
The principle determinants of ETCO2 are alveolar ventilation, pulmonary
perfusion (cardiac output) and CO2 production (Benumof, 1998; Callaham &
Barton, 1990; Domsky, Wilson & Heins, 1995; Steedman & Robertson, 1990).
During acutely low cardiac output state as in cardiac arrest, decreased
pulmonary blood flow becomes the primary determinant resulting in abrupt
decrease of ETCO2 (Domsky et al., 1995; Wayne et al., 1995). Changes in
alveolar ventilation can also influence ETCO2 as PACO2 closely approximates
PaCO2 and ETCO2 (Santos et al., 1993). If ventilation and chest
compressions are constant with the assumption that CO2 production is
uniform, then the change in ETCO2 reflects the changes in systemic and
pulmonary blood flow (Garnett et al., 1987). Ultimately, ETCO2 can be used
as a quantitative index of evaluating adequacy of ventilation and pulmonary
blood flow during CPR (Falk et al., 1988).
ETCO2 Monitoring Technologies
One way of measuring ETCO2 is with the infrared capnometer, which contains
a source of infrared radiation, a chamber containing the gas sample, and a
photodetector (Santos et al., 1993; Trillo et al., 1994). When the expired
CO2 passes between the beam of infrared light and photodetector, the
absorbence is proportional to the concentration of CO2 in the gas sample
(LaValle & Perry, 1995; Santos et al., 1993; Trillo et al., 1994). The gas
samples can be analyzed by the mainstream (in-line) or sidestream
(diverting) techniques (Santos et al., 1993).
The mainstream capnometer uses the airway connector placed in-line with the
patient’s breathing circuit directly attached to endotracheal tube (Santos
et al., 1993).This technique produces instantaneous and accurate gas
analysis (less than 500 msec) far superior to the sidestream technique
(Callaham & Barton, 1990; Santos et al., 1993). The limitation of the
mainstream technique is that it can be applied only for intubated patients
or patients with tight fitting nose or face masks (Santos et al., 1993). On
the other hand, the sidestream technique is more applicable for
spontaneously breathing non-intubated patients. But, it requires constant
aspiration of 100 cc to 300 cc of expired air/minute for analysis (Santos
et al., 1993).
ETCO2 analyzer adapters do not interfere with ventilation (Santos et al.,
1993). However, there are several factors that can alter ETCO2 measurements
such as temperature of photo detector, airway pressure, calibration error,
contamination of sample chamber by moisture and secretion (LaValle & Perry,
1995; Sanders, 1989). Furthermore, falsely high or low ETCO2 measurements
can be resulted by buffer agents (i.e. NaHCO3), recent ingestion of
carbonated beverages, antacids, a-agonists (i.e. epinephrine) and mask
ventilation with CO2 containing gases such as nitrous oxide (Benumof, 1998;
Sanders, 1989; Santos et al., 1993; Trillo et al., 1994).
An alternative to capnometer is a disposable ETCO2 detector, a colorimetric
chemical indicator (Santos et al., 1993). This is a qualitative measurement
of ETCO2 that changes color in the presence of CO2 (i.e. purple to yellow
with presence of CO2). This paper will only address studies, which utilized
capnometers to measure ETCO2 during CPR in ED and prehospital setting.
Research Critique: Experimental Studies
Before 1990, numerous experimental animal studies attempted to identify the
relationship between ETCO2 and CO. An early experimental study by Sanders
et al.(1985) attempted to determine if ETCO2 measurement during CPR could
be used as a prognostic indicator of successful resuscitation from cardiac
arrest in animal model. Using the time series design, the researchers
measured ETCO2 during different phases of resuscitation (Wilson, 1989).
This experimental study has qualities of manipulation, control and
randomization (Polit & Hungler, 1995). Twelve healthy mongrel dogs (mean
weight 11.3 ± 1.9 kg) were anesthetized with pentobarbital and
endotracheally intubated. A capnometer was attached to the endotracheal
tube (ETT) to record ETCO2 with each respiration. Catheters were inserted
through femoral arteries and veins to reach the heart. Postmortem
examination confirmed catheter placement. After the dogs were electrically
fibrillated with 50 Hz through the pacing catheter, chest compressions and
assisted ventilation (5:1 compression/ ventilation ratio) were started
using the mechanical resuscitator. Half of the dogs received high pressure
chest compressions (80 lb.) and half received low pressure compressions (40
lb.). Epinephrine 0.5 mg was given at 3, 6, 9, and 12 minutes (min) of
ventricular fibrillation (VF). After 15 min of chest compressions and
assisted ventilation, animals were defibrillated with 80J. Data on ETCO2,
aortic pressure, right atrial pressure, and ECG were recorded. The process
for calibration for all these instruments was not found in the article. The
mean and standard deviation of ETCO2 and coronary perfusion pressure (CPP)
at each minute of VF were calculated for resuscitated and nonresuscitated.
For the remainder of this paper, the word return of spontaneous circulation
(ROSC) will be used in describing resuscitated subjects.
For statistical analysis, two-tailed Student t test was used to detect the
significant difference (P<.05) between ETCO2 of animals with ROSC and
without ROSC at each minute of VF. According to Wilson (1989), t test for
continuous variables is appropriated selection for this experimental study.
There was a significant difference between ROSC and without ROSC animals in
the overall mean ETCO2 (9.6 ± 3.2 mmHg vs. 3.2 ± 1.1 mmHg). Linear
regression analysis was done to determine the relationship of ETCO2 to CPP
during CPR. ETCO2 was highly correlated with CPP (r=.91; P<.01). Thus, it
was concluded that CPP could be predicted from ETCO2 measured in this
sample. This study used healthy dogs in which VF was induced artificially.
Therefore, the applicability of these findings to the resuscitation of
patients with cardiac and pulmonary diseases is questionable. Also,
thoracic cavity is different in dogs; thus, chest compressions may produce
different results. Future clinical studies are required for validation of
these findings. Lacking routine measurements of arterial blood pressure and
tidal volumes as part of the procedure evidenced some of the limitations of
this study. It is possible that differences in these parameters may have
influenced ETCO2. However, the measurements were not analyzed by the study;
thus, the potential relationship is unknown.
Gudipati et al. (1988) also conducted an experimental time series study to
investigate the potential usefulness of ETCO2 as a prognosticator of
resuscitability. Minnesota mini pigs (N=22; weight 20-35 kg) were
anesthetized with ketamine, pentobarbital sodium and pancuronium, a
blocking agent. The pigs were intubated and mechanically ventilated with a
set rate, tidal volume and mix flow rate. Femoral arteries and veins were
used to insert pressure monitoring catheters to reach the heart. All
instruments and procedures were thoroughly described in the article, but
the description of ETCO2 analyzer calibration was not found in the article.
For the ETCO2 measurement, a sidestream analyzer was attached to the ETT.
CO was measured by the thermodilution technique. Before initiating CPR for
cardiac arrest of ventricular fibrillation (VF), CO, ETCO2, aortic and
right atrial pressures were monitored with pulmonary arterial and aortic
blood gases. A current of 5 mA was delivered to the right ventricle to
induce VF. Cardiac arrest was confirmed by VF on ECG with a decline in
aortic systolic pressure to less than 25 mm Hg and decline in pulse
pressure to less than 5 mmHg. At that time, the FIO2 was increased to 100%
to maintain PaCO2 of 35-45 mmHg. The ventilator and compressor delivered
5:1 compression/ventilation ratio. Thumper, a programmable cardiopulmonary
resuscitator, delivered a set rate of compression with equal interval and
depth at a regular cycle. At 1, 5, and 9 min during CPR, CO and ETCO2
measurements were obtained. After 12 min of CPR, countershocks (40, 80, 160
and 320 J) were applied to the anterior chest with a defibrillator. If
animals were successfully resuscitated, CO measurements were repeated at 6
min after resuscitation.
The second part of the experiment consisted of laparotomy (N=5), creating a
window with a midline incision on pigs, who received same anesthesia, mode
of ventilation and chest compressions. After 1 min of VF, direct cardiac
massage was performed through the window for 5 min. Then, defibrillation
with unknown amount of direct-current countershock was attempted. During
this procedure, ETCO2 was continuously monitored and cardiac index (CI) was
measured at 1 and 5 min after the initiation of direct cardiac massage. For
statistical analysis, the difference in CI and ETCO2 between animals with
ROSC and without ROSC were analyzed by the Student t test for unpaired
measurements. This test was appropriate for testing the difference between
the means of two independent groups (i.e. ROSC vs. without ROSC) (Norman &
Streiner, 1997). The measurements of ETCO2 in ROSC and without ROSC animals
were analyzed by repeated measurement analysis of variance by Wilk’s
method. According to Polit and Hungler (1995), this test is used when there
are three or more measures of the same dependent variable for each subject.
For example, this type of test is used when multiple measures of the same
dependent variables are collected longitudinally at several points in time
(Polit & Hungler, 1995). With linear regression analysis, the correlation
between ETCO2 and CI was analyzed as one independent variable (CI) was used
to predict the dependent variable (ETCO2) (Polit & Hungler, 1995). The
results showed a rapid increase in ETCO2 after ROSC. At 1 and 9 min after
precordial compressions, the CI averaged 27 ± 1% and 38 ± 4% of prearrest
values, respectively; ETCO2 averaged 27 ± 5% and 43 ± 8% of precardiac
arrest value. After 6 min of spontaneous circulation, CO increased to 88 ±
5% and ETCO2 increased to 121 ± 80% of precardiac arrest value. There was a
significant difference in the average ETCO2 of the animals with ROSC and
without ROSC (N=7 with ROSC, 1.7 ± 0.2%; N=5 without ROSC, 0.5 ± 0.1% ,
P<.001). The correlation between ETCO2 and CO for 22 animals averaged .92 ±
.07 (ranged from .75 to .99; p<.001).
For open chest cardiac massage of 5 animals, ETCO2 and CI were measured
before cardiac arrest, 1 and 5 min after beginning direct cardiac massage,
and after ROSC. The researchers also reported similar proportional changes
in ETCO2 and CI in the open chest animals. The correlation coefficients
from the relationship between ETCO2 and CI for 5 animals ranged from .91 to
.98 (mean .95 ± .014). This study showed that ETCO2 could be a noninvasive
measure of pulmonary blood flow reflecting CO. Furthermore, ETCO2 was shown
to identify ROSC and helped predict outcomes during CPR. Additionally, the
dramatic increase in ETCO2 to a level exceeding the prearrest values
provided a definite evidence of ROSC, suggesting that precordial
compressions might not need to be interrupted to assess for ROSC. The
findings in this study are promising but the generalizability to humans is
speculative, requiring clinical trials to confirm its implication in
clinical settings.
Research Critique: In-Hospital Studies (ED)
In the late 1980’s, several clinical studies were conducted in an attempt
to confirm some of the findings from the experimental studies. The study by
Garnett et al. (1987) was one of the first prospective quasi-experimental
time series studies to determine the usefulness of ETCO2 in hemodynamic
monitoring during CPR. The prospective time series design was an
appropriate selection, allowing the researchers to use "before"
measurements to establish a baseline while comparing posttreatment
measurements (Wilson, 1989). According to Polit and Hungler (1995),
quasi-experimental design does not contain a control group lacking
randomization but has some manipulation of the procedure. In fact,
strengths of this design are practicality, feasibility and generalizability
(Polit & Hungler, 1995). Overall, the study design selection was
appropriate. The inclusion criteria for the convenience sample were orally
intubated adults (age ³ 18 years) with atraumatic prehospital cardiac
arrest. The prehospital treatment consisted of basic and ACLS according to
AHA. Upon ED arrival, CPR was continued using Thumper. A calibrated
sidestream capnometer measured ETCO2 continuously. The article indicated
that ETCO2 was reported as the percentage of CO2 in exhaled gas, but the
normal value of CO2 was not stated in the article. The threat to the
reliability and validity of the instrument was controlled by using a
calibrated capnometer. ROSC was confirmed by the detection of pulse rate
and audible or palpable blood pressure. Of twenty-three patients, whom had
ETCO2 recorded during resuscitation, ten patients had ROSC. For data
analysis, unpaired Student t-test appropriately compared the means of ETCO2
in the two groups: the group with ROSC and without ROSC (Norman & Streiner,
1997; Polit & Hungler, 1995). Paired Student t test compared two paired
observations (ETCO2 values before ROSC and the peak ETCO2 after ROSC). P<
0.05 was considered significant.
Before ROSC, ETCO2 measurements in the two groups were similar (with ROSC,
N=10, 1.7 ± 0.6% vs. without ROSC, N=13, 1.8 ± 0.9%). In the ROSC group
(N=10), ETCO2 increased so immediately that it was the very first clinical
indicator of any changes in the patient’s status. The ETCO2 of the ROSC
group peaked three times greater than before ROSC within 2-5 min (4.6 ±
1.4%). Then, ETCO2 slowly declined to a stable level (3.1 ± 0.9%).
Therefore, this study suggested that ETCO2 could be useful in predicting
the positive outcome of CPR. The potential limitation of this study was
that error could be introduced by the technological difficulties from
Thumper or the method of mechanical ventilation. Although the sample size
was small, the findings were generalizable to the ED settings, where ETCO2
could be used to guide the treatment during resuscitation after atraumatic
cardiac arrest.
Sanders et al.(1989) conducted the first clinical trial to determine if
ETCO2 could be used as the prognostic indicator for ROSC. A convenience
sample from two hospitals was included in this study. The inclusion
criteria were the same as the previous study by Garnett et al. (1987). The
exclusion criteria were described as traumatic cardiac arrest, invasive
CPR, and ROSC after defibrillation without the need for intubation.
Following intubation, a calibrated mainstream ETCO2 analyzer was placed
between ETT and resuscitation bag. Manual ventilation presented a threat to
the internal validity as hyperventilation could falsely decrease ETCO2
(Callaham & Barton, 1990). ETCO2 measurements obtained five min after
NaHCO3 administration were eliminated from the analysis due to the
potential for a false increase in ETCO2 measurements. For data analysis,
unpaired two tailed Student’s t test was used to compare the means of
continuous variables (i.e. ETCO2). To determine the association of the
nominal data (i.e. initial cardiac rhythm) with ROSC group, chi square
analysis was used appropriately. Linear logistic regression is a procedure
that analyzes the relationship between multiple independent variables (i.e.
ETCO2 values at different time intervals) and the categorical dependent
variable (ROSC vs. without ROSC) (Polit & Hunger, 1995). This test was
appropriately used to evaluate the predictive effect of ETCO2 (independent
variable) on patients with ROSC (yes/no-categorical dependent variables).
Of 133 eligible patients, only 35 patients were continuously monitored with
capnometry and were eligible for analysis. Nine patients with ROSC had a
mean ETCO2 of 15 ± 4 mmHg, which was greater than the mean ETCO2 for 26
patients without ROSC (7 ± 5 mmHg). The mean ETCO2 of ROSC group at 11 to
15 min was 17 ± 4 mmHg, whereas the mean ETCO2 for the group without ROSC
was 9 ± 7 mmHg (P=.04). At 16 to 20 min, the difference between two groups
further increased to 18 ± 6 mmHg vs. 6 ± 3 mmHg (P=.0004). All patients
(N=9) with ROSC had the ETCO2 ³ 10 mmHg, but six patients without ROSC had
ETCO2 of 10 mmHg. Sanders et al. (1989) explained that, despite adequate
perfusion pressure for resuscitation, severe myocardial or coronary disease
can prevent successful resuscitation. Therefore, one can conclude that
ETCO2 greater than 10 mmHg do not guarantee a successful resuscitation. In
fact, the threshold of 10 mmHg may not be generalizable for all patients,
especially those with comorbidities. However, ETCO2 of 10 mmHg as a
prognostic threshold value produced a sensitivity of 100% and a specificity
of 77%, positive predictive value of 60% and negative predictive value of
100% in this study. For the initial cardiac rhythm, VT/VF were associated
with survival (P<.05) and asystole/EMD were associated with nonsurvival
(P<.05). As pointed out by the authors, the generalizability could be
limited by the potential inconsistency of instrumentation and collecting
data on ETCO2 measurements in the two hospitals. Additionally, the chest
compressions and ventilation were not quantified, which could effect ETCO2.
The overall findings from the study by Sanders et al. (1989) concluded that
ETCO2 could be used as a prognostic guide during CPR after atraumatic
cardiac arrest.
Callaham and Barton (1990) also investigated the utility of ETCO2 as a
predictive measure of initial outcome of resuscitation (i.e. ROSC) using
the same study design and sample selection. The eligible patients (N=55)
were atraumatic prehospital cardiac arrest victims, who were transported to
the ED, where the study was conducted (age, 69.9 ± 12.2; N=35 male, 64%).
The prehospital treatment included basic/advanced life support according to
AHA. In the ED, patients were resuscitated by the most senior physicians,
who were not aware of the possible significance of ETCO2 during this study
period. Orally intubated patients were manually ventilated, which
introduced a threat to the internal validity for lacking consistent control
of the ventilation. Thumper delivered chest compressions (80/min with 50%
compression cycle). Callaham and Barton (1990) used a calibrated mainstream
capnometer for obtaining ETCO2. The main focus were the initial values of
ETCO2, which were obtained both within five min of ED arrival and after one
min of ventilation. The frequency of ‘regular interval’ monitoring and
recording of ETCO2 were not defined in the article. For statistical
analysis, unpaired two tailed Student’s t-test compared the initial ETCO2
values of the two groups (with ROSC and without ROSC). Fourteen of 55
patients had ROSC. The mean initial ETCO2 of ROSC group, whose ETCO2
measurements were obtained both within five min of ED arrival and after one
min of ventilation, was three times higher than the group without ROSC (19
± 14 mmHg vs. 5 ± 4 mmHg, P<.0001). An initial ETCO2 of 15 mmHg correctly
predicted ROSC with a sensitivity of 70%, specificity of 98%, positive
predictive value 91% and negative predictive value of 91%. The threshold of
15 mmHg was deduced by plotting the ETCO2 values on the receiver operating
curve. For the entry cardiac rhythm, there was a significant ROSC in
patients presenting with asystole (P<.035) and EMD (P < .01) and compared
to VF/VT. This finding was inconsistent with Sanders et al.(1989), who
reported that asystole/EMD were associated with nonsurvival (P<.05).
Callaham and Barton (1990) concluded that the initial predictive value of
15 mmHg was not limited to a particular rhythm. A potential threat of
Hawthorne effect (Polit & Hungler, 1995) could have caused the physicians
to perform more aggressive resuscitation on patients in this study although
the physicians were not aware of the significance of ETCO2. Furthermore,
inadequately controlled manual ventilation could have potentially affected
ETCO2. The generalizability of the findings from this study is limited to
the ED population of atraumatic cardiac arrest without comorbidities such
as COPD and ARDS. This study also demonstrated that a sudden rise of ETCO2
often was the first indication of ROSC as seen in the studies from Garnett
et al. (1987). Additionally, Callaham and Barton (1990) were able to deduce
a predictive relationship between ETCO2 and the positive outcomes from CPR
as did Sanders et al. (1989).
Steedman and Robertson (1990) in United Kingdom (UK) assessed the clinical
applicability of ETCO2 measurement during CPR in the ED using the same
study design and sample selection as the previously described studies. The
major difference was that patients received only basic life support in the
field. Upon arrival to the ED, the patients were orally intubated and
ventilated with 100% oxygen. The calibrated mainstream capnometer monitored
ETCO2 continuously and reported the values as the percentage of CO2 in
exhaled gas. Steedman and Robertson (1990) controlled the potential threats
to the internal validity by using a Thumper and mechanical ventilation. The
paired t test was used to compare ETCO2 before and after ROSC. The unpaired
t-test compared the means of ETCO2 in patients with and without ROSC.
Of the small sample size of 12 patients (age 69 ± 17; N=8 male), five
patients had ROSC. In the ROSC group, ETCO2 gradually increased from 1.8 ±
.92% to 3.38 ± 1.06% within one min (p < 0.05). ETCO2 reached its peak
value (3.7 ± 1.08%) at two min. A stable level of ETCO2 (3.02 ± 0.52%) was
maintained after a slight drop from the peak value at eight min or more of
ROSC. Similar phenomenon was also reported by Garnett et al.(1987). ETCO2
measurements were significantly different (P<0.001) between patients with
and without ROSC (N=5, 2.63 ± 0.32%; N=7, 1.64 ± 0.89%, respectively). ROSC
group in this study showed a two-fold increase in ETCO2. Four patients
received a mean dose of 100 mEq NaHCO3 but did not show any statistical
difference in ETCO2 (1.5 ± 0.49% to 1.8 ± .54%; P value was not available).
One of the limitations of this study was that ACLS was not performed in
prehospital, and the impact of this factor was not analyzed. The findings
from this study confirmed the similar results from three previous studies,
even though there was a small sample size. Therefore, the generalizability
is evident. Steedman and Robertson (1990) concluded that ETCO2 monitoring
could provide a useful noninvasive method to assess the effectiveness of
blood flow produced by precordial compression after atraumatic cardiac arrest.
Research Critique: Prehospital Studies
Emergency medical service personnel rely on ECG rhythm, down time, time
elapsed from CPR and the patient’s medical history as a prognosticator
since there are no reliable data (Aspline & White, 1995). Aspline and White
(1995) conducted a study to determine the prognostic significance of
initial ETCO2 measurement and to explore the role of capnography in the
management and outcome of out of hospital cardiac arrest (OHCA). The
purpose of this study was to test the hypothesis that initial ETCO2
measurements are higher in patient with ROSC during CPR and are therefore
prognostic for ROSC in patients with OHCA. This was a prospective time
series design looking at a convenience sample (N=34) of atraumatic OHCA
over 13 months. According to the ACLS guidelines, the cardiac arrest
victims were intubated endotracheally and continuously monitored with a
mainstream analyzer. The ETCO2 analyzer was calibrated according to the
manufacturer’s guideline. Automated ventilation, which was oxygen powered
and time cycled, was used to maintain ventilation (10-12 per min with tidal
volume of 600-800 ml). Since this was not a blinded study, having the
automated ventilation was a good control for the internal validity. Without
this control, the participants might aggressively bag the first 1-2 min to
achieve a high initial ETCO2. The initial ETCO2 was recorded after 1-2 min
of monitoring, and the maximum ETCO2 was recorded. Due to the potential
effect of NaHCO3 on ETCO2, no ETCO2 within 5 min of NaHCO3 administration
was documented for the analysis. This also was a good control for the
threat to internal validity. For data analysis, one-tailed t test was used
to compare the initial and maximum ETCO2 between the two groups (with ROSC
and without ROSC). P £ .05 was considered significant. The one tailed test
was appropriate since the hypothesis was testing the higher value of ETCO2.
ETCO2 measurements were documented only on 34 patients out of 65 patients.
The potential problem related to the attrition was not addressed in the
article. Of 34 patients, seven patients had ROSC before capnometry
monitoring was started; thus, ETCO2 was not measured. The final 27 patients
had ETCO2 readings available during CPR. After 1 min, ETCO2 in 14 patients
with ROSC was significantly higher than patients without ROSC (23.0 ± 7.4
mmHg vs. 13.2 ± 14.7 mmHg, P=.0002) as seen in the study by Callaham and
Barton (1990). During CPR, the maximum value was higher in patients with
ROSC than patients without ROSC (30.8 ± 9.5 mmHg vs. 22.7 ± 8.8 mmHg,
P=.0154). Only three patients were survived to hospital discharge, but
their neurological status was not described in the article. The usefulness
of ETCO2 monitoring as a prognosticator for ROSC was promising but
questionable, due to the small convenience sample size and small survival
patients. Therefore, a larger sample is recommended.
Wayne et al.(1995) conducted a study to evaluate the quantitative
measurement of ETCO2 in prehospital setting and to determine whether this
value could be used as a marker to predict death. This study was a
prospective time series design looking at patients (N=90, 61 males; age
67.6 ± 13.6), who were victims of normothermic and atraumatic pulseless
electrical activity (PEA). The reason for selecting PEA as an inclusion
criterion was not described in the article. The exclusion criteria were
having VF or VT. All samples were intubated and connected to a
self-calibrated mainstream ETCO2 analyzer and ventilated by a standard
adult bag valve mask. Using manual ventilation introduced a threat to the
internal validity. The termination of resuscitation was based on the
presence of persistent ETCO2 level of 10 mmHg or less after 20 minutes of
ACLS. The researchers explained that an ETCO2 level of 10 mmHg represented
less than 1% of CO2 production and was thus incompatible with life. But in
reality, due to potential survival, the resuscitation went on until loss of
electrical activity or ROSC, resulting in prolonged effort of CPR. For the
analysis, Wilcoxin rank sum test was used for ordinal data. This test
involves taking the difference between paired scores and ranking the
absolute difference (Polit & Hungler, 1995). It is a nonparametric
equivalent of the paired t test to compare group mean (i.e. initial,
minimum ETCO2). The logistic regression was appropriately used to see the
association between ETCO2 and survival to hospital discharge.
Seven out of 16 patients, who had ROSC, were discharged from the hospital.
Four of the seven patients were neurologically intact; three had some
neurologic impairment but were able to care for themselves. According to
the results, the initial ETCO2 for the patients without ROSC was 11.7 ± 6.6
mmHg vs. 10.9 ± 4.9 mmHg with ROSC. After 20 min of ACLS, the average ETCO2
in the group without ROSC was 3.9 ± 2.8 mmHg and 31 ± 5.3 mmHg with ROSC
(P<.0001). In 13 patients, the rise in ETCO2 was the first indication of
ROSC before palpable pulse or blood pressure. Following this analysis,
Wayne et al. (1995) hypothesized that the ETCO2 measurement £ 10 mmHg was a
predictive value for death in the field. The study reported that no
patients survived with ETCO2 less than 10 mmHg. At 20 min of ACLS, this
threshold value of ETCO2 was accurate in predicting death in patients with
atraumatic PEA. However, ETCO2 did not discriminate between the long term
survivors and those who were deceased in hospital. The limitation of this
study was that it contained a small sample size for prospective study.
Further study with a large sample in different population would be
required. Secondly, epinephrine did not effect the study results although
other studies reported its decreasing effect on ETCO2. Thirdly, there was a
potential for threat to the validity due to an interpreter variability in
maintaining consistent minute ventilation using a bag valve device. Future
studies confirming the accuracy of ETCO2 monitoring as a prognosticator of
death or survival can help prevent futile efforts of CPR in the field.
Cantineau et al. (1996) conducted a prospective time series study to test
the hypothesis that continuous assessment of ETCO2 during prehospital CPR
allowed distinction between patients with ROSC and without ROSC with a
sensitivity greater than 90%. A convenience sample (N=120: 84 males and 36
females) with atraumatic prehospital arrest were included in the study.
Fire fighters started resuscitation with bag-valve-mask ventilations and
supplemental oxygen and chest compressions according to AHA. An
anesthesiologist placed an ETT in all patients and continued mechanical
ventilation with a set rate and tidal volume. The mechanism of chest
compressions was not described in the article. The pharmacological
interventions were given according to ACLS guidelines. Epinephrine was
given to all patients. NaHCO3 was given for CPR greater than 10-15 min.
Lidocaine and direct shock were administered for patients with VF. ROSC was
defined as sustained blood pressure for at least 30 seconds. There were two
parts to the study. The first part of the study determined a threshold
value of ETCO2 that would be tested on a large scale. Twenty four patients
had the ETCO2 measured with a sidestream analyzer. The ETCO2 analyzer
calibration was not described in the article. There were three categories
of ETCO2 for data collection and analysis: an initial ETCO2 measurement
after 1 min of mechanical ventilation, minimum ETCO2 and maximum ETCO2
measurements after the first 20 min after intubation and before ROSC. The
sensitivity and specificity were calculated for each category. With NaHCO3,
the ETCO2 measurements just before and 5 min after medication
administration were included for the analysis. The second part of the study
prospectively evaluated the maximum ETCO2 of 10 mmHg on 96 patients in a
quasi-experimental design. Unlike the first part of the study, ETCO2 was
measured by a mainstream analyzer. The reason for changing the technique to
analyze ETCO2 was not described in the article. Having two different
instruments was a threat to the external validity. For statistical
analysis, unpaired student t-test was appropriately used for continuous
data comparison of the independent group (cutoff ETCO2). Chi square for
analyzing the categorical variables was an appropriate method to classify
whether the ETCO2 measurement was below or above categorical groups of
minimum and maximum groups. Student t-test (paired) appropriately analyzed
the difference between the means of the two related groups (i.e. comparing
ETCO2 before and after ROSC, ETCO2 before and after NaHCO3).
For the first part of the study, eight of the 24 patients had ROSC. The
mean ETCO2 measurements were not significantly different in the ROSC or
without ROSC group (16 ± 6.2 mmHg vs. 10.6 ± 8.4 mmHg; P=.12). ROSC was
related to the significant increase in ETCO2 from 26.4 ± 5.4 mmHg to 48.7 ±
13.8 mmHg (P<.01). In the second part of the study, thirty patients out of
96 patients had ROSC. The maximum ETCO2 greater than 10 mmHg predicted ROSC
with a sensitivity of 100% and specificity of 66% after 20 min of
intubation. The maximum ETCO2 less than 10 mmHg was never associated with
ROSC despite 40 min of resuscitation after intubation. Since this study
contained a large number of patients with asystole compared to patients
with VF/PEA, the generalizability of the findings is limited (asystole:
N=109 vs. VF/PEA: N=11). However, this study confirmed the critical
application of ETCO2 monitoring during resuscitation, which could be used
to assess the prognosis of prolonged CPR in the prehospital setting as well
as in the ED.
Critical and Original Analysis of Literature
The overall goal of the previously discussed studies was to determine the
relationship of ETCO2 with CO and to evaluate ETCO2 as a prognosticator of
CPR. In experimental studies, ETCO2 was shown to correlate well with CO,
CPP and resuscitation outcome (Gudipati et al., 1988; Sanders et al.,
1985). As immediate indicator of successful resuscitation in animal models,
this optimistic quality of ETCO2 served as a basis for human application
during atraumatic cardiac arrest.
Applying the significant findings derived from experimental studies, the
usefulness of ETCO2 monitoring and the predictive value of ETCO2 were later
evaluated in clinical settings (Callaham & Barton, 1990; Garnett et al.,
1987; Steedman & Robertson, 1990). The same study design and sample
selection were used in these studies. Common limitations to these studies
were evidenced by using small sample size for the prospective design and
inconsistent method of resuscitation. Garnett et al. (1987) and Steedman
and Robertson (1990) used Thumper and mechanical ventilator, whereas
Sanders et al. (1989) applied manual ventilation and failed to quantify and
indicate the method of chest compression. Callaham and Barton (1990) used
Thumper, but ventilation was not controlled mechanically. Sanders et al.
(1989) and Callaham and Barton (1990) deduced threshold values for
predicting a positive outcome from resuscitation (10 mmHg and 15 mmHg,
respectively). Although Garnett et al. (1987) did not find any prognostic
value for ROSC, the importance of ETCO2 for monitoring blood flow and
guiding the treatment of CPR was confirmed as seen in the studies by
Garnett et al.(1987) and Steedman and Robertson (1990). Callaham and Barton
(1990) explained that the reason why Garnett et al. (1987) did not achieve
the prognostic relationship of ETCO2 was related to using the sidestream
technique. The sidestream technique is less accurate method of sampling
CO2, and the measurement is depended on the location of sampling tube and
the amount of supplemental oxygen (Callaham & Barton, 1990; LaValle &
Perry, 1995).
The prehospital studies also showed the prognostic value of ETCO2 during
CPR and observed similar findings (Aspline & White, 1995; Cantineau et al.,
1996; Wayne et al., 1995). The methods of resuscitation involving
ventilation and compressions varied in each study. Aspline and White (1995)
concluded that the initial ETCO2 could be a prognosticator for ROSC when
automated ventilation was used during CPR. Despite the small sample size,
these findings were similar to the findings from Callaham and Barton
(1990). Similarly, Wayne et al. (1995) deduced a threshold value of less
than 10 mmHg as the prognosticator for irreversible death in OHCA. However,
the generalizability of this finding was limited due to the inclusion
criterion of OHCA with PEA. With a larger sample size (N=120), Cantineau et
al. (1996) conducted a two-part study in establishing that the maximum
ETCO2 value of 10 mmHg had a higher sensitivity (>90%) to predict ROSC in
OHCA of asystole. The generalizability of this finding was limited to
patients with asystole due to the small number of samples with VF/PEA in
the study. Additional threat to the validity of ETCO2 was introduced by
using different types of ETCO2 analyzer. Nonetheless, all three prehospital
studies supported the findings from in-hospital studies, demonstrating the
potential value of ETCO2 as a prognosticator and as a guiding tool for the
effectiveness of CPR.
Integration and Synthesis
Achieving the threshold value for prognostic determination was the most
challenging and difficult accomplishment for all the studies discussed.
Sanders et al. (1989) reported a mean ETCO2 of 15 mmHg for patients with
ROSC and a mean of 7 mmHg for patients without ROSC. The threshold of 10
mmHg predicted successful resuscitation with a sensitivity 100% and a
specificity of 77%. Similarly, Callaham and Barton (1990) reported a mean
of 19 mmHg for patients with ROSC. Their threshold of 15 mmHg predicted
ROSC with a sensitivity of 71% and a specificity of 98%.
In the prehospital studies, the overall mean value of ETCO2 for ROSC was
higher than the mean value found by the in-hospital studies. For example,
Aspline and White (1995) reported a mean of 23 mmHg for ROSC after 1 min of
resuscitation and 13.2 mmHg without ROSC. Cantineau et al. (1996) reported
a mean value of 24 mmHg for ROSC and a mean value of 13.8 mmHg without
ROSC. The higher values of ETCO2 from prehospital studies may suggest that
the early use of capnography during OHCA reflects differences in the timing
and the physiologic state of cardiac arrest (Asplin & White, 1995). Since
the timing of ETCO2 measurement after cardiac arrest may be a critical
factor, establishing a prognostic value may be difficult, especially when
the optimal time for ETCO2 measurement is unknown (Aspline and White,
1995). Finding the threshold value can potentially minimize the cost and
futile effort for prolonged CPR.
Although ETCO2 monitoring during CPR has a potential ability to predict the
outcomes of CPR, there are several limitations. First, ETCO2 measurements
may be effected by inconsistent methods of manual ventilation and chest
compressions (Steedman & Robertson, 1990). In real life, manual ventilation
and chest compressions could cause ETCO2 to fluctuate with the effort of
compression and rate of ventilation (Sanders et al., 1989; Steedman &
Robertson, 1990). Ideally, the minute ventilation should be controlled
during quantitative monitoring of ETCO2 in cardiac arrest since ETCO2 is
effected by the alveolar ventilation (Idris et al., 1994).
Second, the effect of the resuscitation medications such as NaHCO3 and
epinephrine should be taken into consideration. According to Callaham,
Barton and Matthay (1992), ETCO2 could be decreased inconsistently with
epinephrine, but the predictive value of ETCO2 was not eliminated during
CPR. The exact mechanism of decreasing ETCO2 after epinephrine
administration is unknown (Callaham et al., 1992). The effect of higher
dose of epinephrine remains questionable and requires further study.
Concerning the effect of NaHCO3 on ETCO2, this medication has proven no
benefits in cardiac arrest and should be avoided especially when monitoring
ETCO2 (Callaham, 1990; Callaham et al., 1992). NaHCO3 is known as a buffer
agent, which can transiently increase ETCO2 but the measurements return to
perfusion level within 5 min (Trillo et al., 1993).
Third, the studies reported conflicting findings of cardiac rhythms that
were associated with ROSC. According to Sanders et al. (1989), the initial
cardiac rhythms of VT/VF were associated with ROSC, and asystole/EMD were
associated with nonsurvival (no ROSC). However, these findings were
inconsistent from Callaham and Barton (1990), who reported that asystole
/EMD were significantly associated with the outcome of ROSC. The analysis
from prehospital studies did not support these findings. Wayne et al.
(1995) only assessed patients with PEA and excluded VF/VT. The rational for
the exclusion criterion was not found in the article. In addition, the
findings from the study by Cantineau et al. (1996) were applicable to
patients with atraumatic cardiac arrest of asystole.
Lastly, atraumatic cardiac arrests can be frequently caused by acute and
chronic illness with comorbidities. As discussed previously, when
ventilation and perfusion are equal, PaCO2 is equivalent to ETCO2 (LaValle
& Perry, 1995). However, conditions such as COPD or ARDS result in a VQ
abnormality and high CO2 gradient, which causes PaCO2 to change and make it
difficult to assess the accuracy of ETCO2 (LaValle & Perry, 1995; Levin &
Pizov, 1997; Santos et al., 1993). The potential implication of ETCO2
monitoring under these circumstances including traumatic cardiac arrest is
limited as evidenced by lack of studies looking at the different groups of
patients.
Application
Currently, ETCO2 monitoring is widely used for various clinical practices
such as verification of endotracheal tube placement, assessment of
conscious sedation safety and evaluation of mechanical ventilation (LaValle
& Perry, 1995; Sanders, 1989; Santos et al., 1993). ETCO2 monitoring can
guide nurses in providing adequate oxygenation and ventilation to unstable
patients if capnography is used correctly (LaValle & Perry, 1995). For
example, ETCO2 monitoring in conjunction with ABG’s are useful for ensuring
adequate ventilation for patients with head injuries (Sanders, 1989). A
fall in ETCO2 may mean decrease in lung perfusion. If ventilation has not
changed, the decrease in ETCO2 may indicate early signs of shock (Sanders,
1989). However, ETCO2 must be interpreted in the context of other
information about the patient’s clinical status.
In the ED, the application of ETCO2 monitoring contributes an additional
valuable asset to the clinical practice, especially during resuscitation.
One can use the feedback from ETCO2 to change the effort (depth/rate/force)
of chest compression during CPR (Lambert et al., 1992). Due to the ability
of ETCO2 to detect ROSC, CPR does not need to be interrupted in order to
establish whether spontaneous circulation has been restored (Steedman &
Robertson, 1990). The use of ETCO2 monitoring in OHCA can potentially
increase the rate of ROSC and survival by instituting earlier monitoring
that could guide the effectiveness of CPR (Aspline & White, 1995).
In conclusion, the critical role of ETCO2 monitoring during CPR has been
demonstrated and confirmed by both experimental and clinical studies. An
ETCO2 analyzer is easy to apply and readily available. As a quantitative
indicator of the volume of blood flow produced by pericardial compressions,
ETCO2 can be a noninvasive method of monitoring the efficacy of ongoing
effort and the outcome of CPR (Falk et al., 1988; LaValle & Perry, 1995;
Sanders et al., 1989).
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"End Tidal Carbon Dioxide Monitoring During CPR: A Predictor of Outcome"
by Jinhee Nguyen, RN MSN [[log in to unmask]]
© Jinhee Nguyen, RN MSN
is presented by Emergency Nursing World ! [http:ENW.org]
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